Effect of cetirizine and prednisolone on cellular infiltration and cytokine mRNA expression during allergen-induced late cutaneous responses


Professor A. B. Kay. Department of Allergy and Clinical Immunology. National Heart & Lung Institute. Dovehouse Street. London. SW3 6LY. UK.


Background The ability of cetirizine to inhibit eosinophil infiltration into the sites of allergen-induced cutaneous late-phase reactions is controversial. A previous skin biopsy study gave negative results with 15 mg of cetirizine as a single dose.

Objective To confirm these findings we have used cetirizine (30 mg daily) for 5 days and compared the results with prednisolone (20 mg daily for 5 days) as a positive control. The efTect of these agents on mRNA positive cells for inlerleukin-3 (IL-3). interleukin-4, interleukin-5 and granulocytc/macrophage-colony stimulating factor (GM-CSF) was also evaluated.

Methods A double-blind, placebo-controlled cross-over study (n= 12) was followed. After each treatment 30 biological units (BUs) of Dermatophagoides pteronyssinus or Phleum pratense were injected inlradermally and the early (15min) and late-phase response sizes (6 and 24h) were measured. Skin biopsies were taken at 24h for immunocytochemistry and in situ hybridization.

Results Cetirizine but not prednisolone inhibited the early-phase response (37%, p = 0.004). In contrast prednisolone. but not cetirizine, significantly inhibited the size of the late-phase reaction at 24 h (70%. P = 0.021). This was associated with significant decreases in tolal (MBP+) and activated (EG2+) eosinophils (P= 0.019 and 0.014, respectively), as compared with placebo. There were also clear but non-significant reductions in interleukin-3, interleukin-4, interleukin-5 and granulocyte/macrophagc-colony stimulating factor mRNA+ cells.

Conclusion Prednisoione, but not cetirizine. inhibited both the magnitude of the allergen-induced late-phase response and the accompanying local eosinophil infiltration. These corticosleroid effects were associated with a reduction in cells expressing mRNA for ‘TH2-type’ cytokines.